Mission

Neurology Networks tries to offer broad exposure to various topics that may be presented on the veterinary neurology board exam.

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MRI

“Dynamic magnetic resonance imaging of the normal canine pituitary gland.”

Graham JP, Roberts GD, Newell SM.

Vet Radiol Ultrasound. 2000 Jan-Feb;41(1):35-40.

Abstract

The pituitary glands of six normal dogs were evaluated using dynamic magnetic resonance imaging. T1 weighted images were obtained every 13 seconds for three minutes of three contiguous slices through the pituitary gland following a bolus intravenous injection of gadolinium-DTPA. Contrast enhancement was seen initially in the region of the pituitary stalk at 52-65 seconds followed by uniform enhancement at 104-143 seconds post injection. This pattern of enhancement was seen in all subjects and is similar to that reported in humans

 

 

“Measurement of interthalamic adhesion thickness as a criteria for brain atrophy in dogs with and without cognitive dysfunction (dementia)”

Hasegawa et al.

VRUS, Vol 46, No 6, 2005: 452-457

 

78 dogs of various breeds aged 6 months-18 years. Average ITA thickness was 6.79+/- 0.70mm in clinically normal dogs versus 3.82+/-0.79mm in clinically demented dogs.

 

Other typical signs of age-related brain atrophy include:

  1. Enlargement of the ventricular system
  2. Well-demarcated sulci (enlargement of the subarachnoidal space)
  3. Diffuse and scattered T2 hyperintensity lesions in the periventricular white matter

1 and 2 come from parenchymal atrophy. T2 hyperintensity can come from myelin degeneration, gliosis, or enlarged Virchow-Robin spaces.

While smaller dogs had overall smaller ITA thicknesses, the only statistically significant correlation was between dogs with dementia and behaviorally normal dogs. A study looking at lysosomal storage disease documented progressive decrease in ITA size suggesting this can be a good measure of parenchymal loss. Another differential can include increased pressure from obstructive hydrocephalus as was noted in a separate case of a Golden with cerebellar meningioma and small ITA measurement presumed to be associated with intracranial pressure changes related to CSF flow obstruction.

 

 

Magnetic resonance imaging contrast enhancement of the trigeminal nerve in dogs without evidence of trigeminal neuropathy.”

Pettigrew R, Rylander H, Schwarz T.

Vet Radiol Ultrasound. 2009 May-Jun;50(3):276-8.

Abstract

Brain magnetic resonance images from 42 dogs imaged between 2002 and 2007 were reviewed retrospectively to establish the incidence of trigeminal nerve contrast enhancement. These dogs had otherwise normal MR images and no clinical evidence of trigeminal nerve disease. Contrast enhancement of the entire trigeminal nerve was seen in 39 dogs and in the region of the trigeminal ganglion in all 42 dogs. When contrast enhancement of the trigeminal nerve was observed, the intensity was subjectively less than or equal to that of the pituitary gland. Contrast enhancement of the trigeminal nerve was seen in 42 dogs with no clinical evidence of trigeminal nerve pathology.

 

 

“MRI Findings in a Rottweiler with Leukoencephalomyelopathy”

Joseph S. Eagleson, DVM, DACVIM (Neurology)*, Marc Kent, DVM, DACVIM (Neurology), Simon R. Platt, BVM&S, DECVN,DACVIM (Neurology), Raquel R. Rech, DVM, DACVP, PhD, Elizabeth W. Howerth, DVM, DACVP, PhD

JAmAnimHosp Assoc 2013; 49:255–261

 

 

A 22 mo old male rottweiler presented with a 1 mo progressive history of general proprioceptive ataxia and upper motor neuron tetraparesis. Neurologic examination was consistent with a lesion affecting the first through fifth cervical spinal cord segments. MRI disclosed bilaterally symmetric hyperintensities on T2-weighted images in the crus cerebri and pyramidal tracts of the brain and the dorsal portion of the lateral funiculi of the cervical spinal cord. Fifty days after initial presentation, the dog was euthanized due to disease progression. Pathologic examination of the central nervous system (CNS) revealed a bilaterally symmetric chronic leukoencephalomyelopathy (LEM) consistent with previous reports of LEM in rottweilers. To the authors’ knowledge, this is the first report to describe the MRI characteristics of LEM in the rottweiler. The topography of the changes observed with MRI paralleled the pathologic changes, which were widespread loss of myelin, decreased axon numbers, and astroglial proliferation.

Conclusion:  MRI of the CNS of affected rottweilers may aid in establishing a presumptive antemortem diagnosis of LEM.

 

**Neuropath details: 

Severe loss of myelin and astrogliosis was found on pathology.  Further, microscopic investigation in the present case using immunohistochemistry (i.e.antibodies against MBP, neurofilament, and GFAP) and electron microscopy corroborated severe myelin loss, astrogliosis/astrocytosis, as well as demonstrating decreased numbers and degeneration of axons. In addition, minimal abortive attempts of oligodendroglial and Schwann cell remyelination were present ultrastructurally. Interestingly, Schwann cells have not be observed in the spinal cord in previously reported cases of LEM.  Schwann cell invasion into the spinal cord can occur in a variety of conditions, including primary myelin disorders as well as focal compressive and concussive processes. Although typically excluded from the CNS, Schwann cell invasion occurs at transition zones where the peripheral nervous system interfaces with the CNS, such as the dorsal and ventral root entry zones and near blood vessels.  Consistent with this, Schwann cells in the present case were observed near blood vessels

 

**The cause of LEM is unknown and thought to be hereditary in rottweilers.  The following have proved negative for inborn errors of metabolism:  b-galactosidase, b-hexosaminidase, b-hexosaminidase A, aryl sul-phatase A, acid phosphatase, b-glucuronidase, a-mannosidase, a-fucosidase, b-glucocerebrosidase, b-galactocerebrosidase, and sphingomyelinase.

FIGURE 1 Transverse plane T2-weighted MRI of the second cervical vertebral (A) and fourth cervical vertebral (B) spinal cord segments, the medulla oblongata (C) and corresponding gross spinal cord specimen from the fourth cervical vertebra (D) from of a 22 mo old male rottweiler with general proprioceptive ataxia and upper motor neuron tetraparesis.

There are bilaterally symmetrical, hyperintense lesions in the dorsolateral funiculi of the spinal cord (arrows in A and B). Images were acquired 50 days after initial presentation.A, B:Insets are from the MRI performed on initial presentation. In the caudal medulla oblongata, symmetrical hyper-intensities also are observed in the pyramids of the medulla oblongata (arrows in C). At the level of the fourth cervical vertebra, the hyperintensities corresponded to bilaterally symmetric opaque foci (arrows) on gross sections (D)

 

 

 

 

 

 

 

 

 

FIGURE 2 Transverse gross and microscopic sections of the spinal cord at the level of second cervical vertebra from the 22 mo old male rottweiler in Figure 1 reveal lesions involving the white matter.

A: Similar to Figure 1D, gross transverse section of the cervical spinal cord at the level of the second cervical vertebra, bilaterally symmetric white foci are also evident in the dorsal area of the lateral funiculi (arrows).

B:On a low power magnification of a transverse section of the cervical spinal cord, there are bilaterally symmetric areas of pallor in the lateral funiculi (arrows). Hematoxylin and eosin staining, bar¼2 mm.  Inset of B: A transverse section of the cervical spinal cord from banked tissue from an age matched control dog. Bar ¼ 2 mm. Note the uniform staining of the white matter.

C:The bi-laterally symmetric areas of pallor in the dorsal areas of the lateral funiculi indicate loss of myelin (arrows). Luxol fast blue staining, bar¼2 mm.  Inset of C: A transverse section of the cervical spinal cord from banked tissue from an age matched control dog. Note the uniform staining of the white matter. Bar¼2mm.

D:The loss of myelin is replaced by gliosis with numerous gemistocytic astrocytes (arrows). In the affected areas, vessels are prominent with hyper-trophy of the endothelial cells (arrowheads). Hematoxylin and eosin staining, original magnification3400, bar¼40 mm

 

FIGURE 3 Microscopic sections of the demyelinated area of dorsolateral lateral funiculus of the first cervical vertebral spinal cord segment from the affected rottweiler compared with the white matter of a similar area of the cervical spinal cord from banked tissue samples from an age matched control dog free of neurologic disease using a variety of immunohistochemical stains.

A: Immunohistochemical stain for myelin basic protein (MBP). In the bilaterally symmetric areas of pallor in the cervical spinal cord, there is severe myelin loss around axons with minimal punctuate positive remnants of myelin. MPB with fast red chromogen/hematoxylin counterstain, original magnification 31000.

B: For comparison, similar location of the cervical spinal cord from a normal dog stained for MBP with fast red chromogen/hematoxylin counterstain, original magnification 31000.

C:Immunohistochemical stain for neurofilament reveals decreased axon numbers. Di-aminobenzidine (DAB) chromogen/hematoxylin counterstain, original magnification31000.

D:For comparison, similar location of the cervical spinal cord from a normal dog stained for neurofilament as in panel C, original magnification31000.

E:Immunohistochemical stain for glial fibrillary acidic protein (GFAP). Myelin loss is replaced by astrocytosis and gemistocytic astrocytes. DAB chromagen/hematoxylin counterstain, original magnification31000.

F:For comparison, similar location of the cervical spinal cord from a normal dog stained for glial fibrillary acidic protein (GFAP) as in panel E. DAB chromagen/hematoxylin counterstain, original magnification31000. Bar¼15 mm

 

FIGURE 4 Electron micrographs from a demyelinated area of dorsolateral lateral funiculus of the first cervical vertebral spinal cord segment reveal axons that are few in number and scattered among oligodendroglial processes.

A: Those axons present are irregularly shaped (A) with wavy decompacted myelin sheaths (M). Lead cit-rate/uranyl acetate staining, bar ¼1mm.

B: Schwann cell remyelination is evident. Myelinated axons (A) are observed surrounded by Schwann cells (S) with basement membrane (arrow). Note the wavy, decompacted myelin (M) and adjacent hypertrophied astrocytic process (As).

Lead citrate/uranyl acetate staining, bar¼1mm

 

 

 

 

 

 

 

 

 

 

 

 

“MRI Findings in a Dog with Kernicterus”

Katie M. Belz, DVM*, Andrew J. Specht, DVM, DACVIM, Victoria S. Johnson, BVSc, DVR, DECVDI, MRCVS, Julia A. Conway, DVM, DACVP

J Am Anim Hosp Assoc 2013; 49:286–292

 

A severe increase in total bilirubin coincided with a decline in neurologic status to comatose in a 9 yr old spayed female mixed-breed dog being treated for immune-mediated hemolytic anemia. The signs started with head bobbing and generalized ataxia which progressed to coma in 4 hours. 

MRI revealed bilaterally symmetrical hyperintensities within the caudate nuclei, globus pallidus, thalamus, deep cerebellar nuclei, and cortical gray matter on T2 and FLAIR sequences, which coincided with areas of bilirubin deposition and neuronal necrosis (kernicterus) identified on necropsy examination.

This is the second case report of an adult dog exhibiting kernicterus, and the first report to document MRI findings associated with that condition. Kernicterus is an uncommonly reported complication of hyperbilirubinemia in dogs, but is potentially underreported due to difficulties in recognizing subtle lesions and distinguishing kernicterus from other potential causes of neurologic abnormalities with readily available antemortem tests. MRI may be helpful in supporting the diagnosis of kernicterus.

**No CSF analysis in this case